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Am J Physiol Lung Cell Mol Physiol 276: L786-L795, 1999;
1040-0605/99 $5.00
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Vol. 276, Issue 5, L786-L795, May 1999

Cyclosporin A protects lung function from hyperoxic damage

E. Matthew, R. Pun, M. Simonich, H. Iwamoto, and J. Dedman

Department of Molecular and Cellular Physiology, University of Cincinnati Medical Center, Cincinnati, Ohio 45267-0576

Cyclosporin A (CsA), an inhibitor of protein phosphatase 2B (calcineurin), has been shown to play a role in exocytosis and neutrophil mobility. Hyperoxia (>95% oxygen for 72 h) causes lung injury and reduces lung compliance. This model is indicative of deficiencies in surfactant and elicits a vigorous immune response leading to further damage. We examined the effects of CsA on surfactant-secreting lung alveolar type II cells. CsA enhances ATP-stimulated increases in whole cell capacitance in the presence of 2 mM extracellular Ca2+. This measurement corresponds with increases in exocytosis. Because of its effect on the immune system and exocytosis from type II cells, CsA was examined for its protective effects against hyperoxia-induced lung damage in mice. We found that CsA (50 mg · kg-1 · day-1) attenuated hyperoxia-induced reductions in lung compliance when administered before or during 72 h of >95% oxygen (P < 0.05). CsA (10 mg · kg-1 · day-1) also had a protective effect against hyperoxia-induced changes in neutrophil infiltration, capillary congestion, edema, and hyaline membrane formation. Wet lung weight-to-dry lung weight ratios did not show any significant changes after hyperoxia or hyperoxia plus CsA (P < 0.05). CsA may be useful to treat patients undergoing prolonged high-oxygen therapy and possibly other lung injuries.

lung compliance; capillary congestion; type I cells; type II cells; hyperoxia; whole cell recording


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